Journal of cardiovascular medicine (Hagerstown, Md.)

Protective mechanism of nicorandil on rat myocardial ischemia-reperfusion.

PMID 22609873


To study the protective mechanism of nicorandil on myocardial ischemia-reperfusion injury. Fifty rats were randomly divided into five groups, four of which were operated on to produce myocardial ischemia-reperfusion. Nicorandil (5 mg/kg) was administrated by intravenous injection to three of the groups. The myocardial ultrastructure was observed by electron microscope. The expression levels of the antiapoptotic protein Bcl-2 and the pro-apoptotic protein Bax were detected by immunohistochemical staining with rhodamine 123. The mitochondrial membrane potential was detected by spectrophotometry. The activity of lactate dehydrogenase (LDH) and malondialdehyde (MDA) content was decreased and the activity of superoxide dismutase (SOD) was increased in the three nicorandil groups, compared with those in the group without nicorandil (P < 0.01, P < 0.05). The positive staining level of the expressed Bcl-2 was increased and the expressed Bax was decreased (P < 0.01) in the three nicorandil groups, compared with those in the group without nicorandil. The mitochondrial inner membrane potential was increased in the three nicorandil groups compared with that in the group without nicorandil (P < 0.05). A suitable level of nicorandil has a protective effect on rats' myocardial ischemia-reperfusion injury, and is mainly based on the opening of the mitochondrial KATP channel and the lowing of Ca overload.

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Nicorandil, ≥98% (HPLC)